Although mass coral bleaching events are generally triggered by high seawater temperatures, experiments have demonstrated that corals and reef-dwelling foraminifers bleach more readily when exposed to high energy, short wavelength solar radiation (blue, violet and ultraviolet [UVR]: Lambda ~ 280 - 490 nm). In seawater, colored dissolved organic matter (CDOM), also called gelbstoff, preferentially absorbs these shorter wavelengths, which consequently bleach and degrade the CDOM. Alteration of watersheds and destruction of coastal wetlands have reduced natural sources of CDOM to reefal waters. I tested the null hypothesis that CDOM does not differ between reefs that differ in coral health, and that water transparency to UVR is not a factor in reef health. I measured absorption of UVR and UV irradiance at various reefs in the Florida Keys that differ in distance from shore and degree of anthropogenic development of the adjacent shoreline. My results show that intact shoreline - associated reefs and inshore reefs tend to be exposed to lower intensities of UVR, and lower degrees of photic stress, than developed shoreline - associated reefs and offshore reefs. Absorption due to CDOM (ag320) was higher, and photic stress, as revealed by increased production of UV-absorbing compounds, Mycosporine - like Amino Acids (MAAs), was lower at the surface compared to the bottom. The following results support my conclusion: ag320 and UV attenuation coefficients (Kd 's) were higher at intact compared to developed shoreline - associated reefs, and at inshore compared to offshore reefs. Spectral slope, S, was higher at offshore compared to inshore reefs, indicating a higher degree of photobleaching of CDOM. Relative expression of MAAs was higher at developed compared to intact shoreline - associated reefs, at offshore reefs compared to inshore reefs, and at the surface compared to the bottom. Solar energy reaching the benthos at two inshore reefs of the same depth (6m) was approximately an order of magnitude higher at the reef near developed shoreline compared to the reef near intact shoreline, and may be due to greater degree of diffuseness of the underwater light field combined with lower ag at the developed shoreline-associated reef.

yes / Skin pigmentation is directed by epidermal-melanin units, characterized by long-lived and dendritic epidermal melanocytes (MC) that interact with viable keratinocytes (KC) to contribute melanin to the epidermis. Previously we reported that MC:KC contact is required for melanosome transfer, that this can be enhanced by filopodial and by UVR/UVA irradiation, which can up-regulate melanosome transfer via Myosin X-mediated control of MC filopodia. Both MC and KC express Ca2+-dependent E-cadherins. These homophilic adhesion contacts induce transient increases in intra-KC Ca2+, while ultraviolet radiation (UVR) raises intra-MC Ca2+ via calcium selective ORAI1 ion channels; both are associated with regulating melanogenesis. However, how Ca2+ triggers melanin transfer remains unclear, and here we evaluated the role of E-Cadherin in UVR-mediated melanin transfer in human skin cells. MC and KC in human epidermis variably express filopodia-associated E-Cadherin, Cdc42, VASP and β-catenin, all of which were upregulated by UVR/UVA in human MC in vitro. Knockdown of E-cadherin revealed that this cadherin is essential for UVR-induced MC filopodia formation and melanin transfer. Moreover, Ca2+ induced a dose-dependent increase in filopodia formation and melanin transfer, as well as increased β-catenin, Cdc42, Myosin X, and E-Cadherin expression in these skin cells. Together these data suggest that filopodial proteins and E-Cadherin, which are upregulated by intracellular (UVR-stimulated) and extracellular Ca2+ availability, are required for filopodia formation and melanin transfer. This may open new avenues to explore how Ca2+ signalling influences human pigmentation.

No description available.